PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “FATTY ACIDS, ESSENTIAL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 469 records · Page 26Linked to original sources
PubMed1995

Effect of essential fatty acid deficiency on membrane fatty acid content and growth hormone stimulation of rat pituitaries during postnatal development.

Fatty acid composition of anterior pituitary cell membranes of rats deprived of essential fatty acids (EFA) and of rats receiving a standard diet was determined during postnatal development and in adults. Pregnant rats were fed an EFA-deficient diet and the offspring were fed the same diet after weaning. In parallel, effects of the diet on growth and on growth hormone (GH) responsiveness to GHRH stimulation were determined in control animals. Membrane content of arachidonic acid (20:4n-6) and of its elongation product adrenic acid (22:4n-6) increased regularly from day 2 to day 12 after birth. EFA-deficiency resulted on day 2 in increased oleic acid and in substitution of arachidonic and adrenic acids by corresponding elongation-desaturation products of oleic acid: eicosatrienoic (20:3n-9) and docosatrienoic (22:3n-9) acids. At the age of 24 days, n-9 series fatty acid reached the same level as in adult animals. Two-day-old EFA-deficient rats paradoxically exhibited a higher level of 20:4n-6 as compared to control rats. EFA-deficiency also decreased growth rate and GH pituitary responses to GHRH during the prepubertal period. These results suggest that changes in the lipid structure and in pituitary secretion properties elicited by EFA-deficiency depend upon the stage of development.

Animals↗
PubMed2000

Essential fatty acids in mothers and their neonates.

Essential fatty acids (EFAs) and their long-chain polyenes (LCPs) are indispensable for human development and health. Because humans cannot synthesize EFAs and can only ineffectively synthesize LCPs, EFAs need to be consumed as part of the diet. Consequently, the polyunsaturated fatty acid (PUFA) status of the developing fetus depends on that of its mother, as confirmed by the positive relation between maternal PUFA consumption and neonatal PUFA status. Pregnancy is associated with a decrease in the biochemical PUFA status, and normalization after delivery is slow. This is particularly true for docosahexaenoic acid (DHA) because, on the basis of the current habitual diet, birth spacing appeared to be insufficient for the maternal DHA status to normalize completely. Because of the decrease in PUFA status during pregnancy, the neonatal PUFA status may not be optimal. This view is supported by the lower neonatal PUFA status after multiple than after single births. The neonatal PUFA status can be increased by maternal PUFA supplementation during pregnancy. For optimum results, the supplement should contain both n-6 and n-3 PUFAs. The PUFA status of preterm neonates is significantly lower than that of term infants, which is a physiologic condition. Because the neonatal DHA status correlates positively with birth weight, birth length, and head circumference, maternal DHA supplementation during pregnancy may improve the prognosis of preterm infants. In term neonates, maternal linoleic acid consumption correlates negatively with neonatal head circumference. This suggests that the ratio of n-3 to n-6 PUFAs in the maternal diet should be increased. Consumption of trans unsaturated fatty acids appeared to be associated with lower maternal and neonatal PUFA status. Therefore, it seems prudent to minimize the consumption of trans fatty acids during pregnancy.

Dietary Fats↗
PubMed1980

Prevention of coronary heart disease: the role of essential fatty acids.

There are 2 classes of essential fatty acids (EFA), the linoleic (n-6) and linolenic (n-3). They are required for the glycerophosphatides (phospholipids) of cellular membranes; the transport and oxidation of cholesterol; the formation of prostaglandins. In deficiency of EFA, cellular membranes are imperfectly formed which causes increased susceptibility to various insults and increased permeability. Low-density lipoproteins (LDL) transport cholesterol mainly as cholesteryl linoleate and supply EFA to tissue. A relative deficiency of EFA (i.e. a high ratio in the body of non-EFA such as long-chain saturated fatty acids to EFA) causes an increase in plasma cholesterol. EFAs cause decreased aggregation of platelets. Atherosclerosis is not caused by increased aggregation of platelets, and can be prevalent in a population in which coronary thrombosis is rare.

Arteriosclerosis↗
PubMed2002

Disturbances in essential fatty acid metabolism in patients receiving long-term home parenteral nutrition.

Patients receiving home total parenteral nutrition (HTPN) are at risk for the development of essential fatty acid deficiency (EFAD). This study examined the essential fatty acid status of patients on long-term HTPN for gut failure. Serum phospholipid and triglyceride fatty acids were measured in 11 patients and 10 healthy volunteers. Patients had similar levels of linoleic acid (18:2w6) in serum triglyceride fatty acids but significantly lower levels of 18:2w6 in serum phospholipids compared to controls. Although there was accumulation of Mead acid (20:3w9) in both fatty acid fractions, the ratio of 20:3w9 to arachidonic acid (20:4w6) remained less than 0.2, reflecting an adequate essential fatty acid status in these patients. There were, however, substantial increases in 20:4w6 content in both triglyceride and phospholipid fractions in serum despite the lower levels of 18:2w6 in serum phospholipids, suggesting that an accelerated hepatic conversion of 18:2w6 to 20:4w6 occurs in HTPN patients, as well as the 20-carbon members of w3 (20:3w3) and w9 (20:3w9) families. The determination of optimal parenteral fat intakes should be investigated further as important priority in patients receiving long term HTPN.

Adult↗
PubMed1981

Metabolism of trans fatty acids with emphasis on the effects of trans, trans-octadecadienoate on lipid composition, essential fatty acid, and prostaglandins: an overview.

Information concerning the metabolism of trans isomers of dietary unsaturated fatty acids is presented. Dietary trans-octadecenoic and trans,trans-octadecadienoic acids are apparently absorbed, activated, oxidized, and acylated into ester lipids much like saturated fatty acids although differences have been observed with regard to their metabolism by different organs. Because of the important role of linoleic acid as the principal precursor of cyclic endoperoxides, prostaglandins and leukotrienes, the potential deleterious effects of trans isomers of this acid are discussed. High levels of dietary trans,trans lineoleate can impair delta 6 desaturase activity and decrease prostaglandin production in rats on experimental diets.

Animals↗
PubMed1982

Metabolic changes in scaly lesions of rat skin produced by essential fatty acid deficiency.

Marked changes in the structure and metabolism of lipids were observed at scaly lesions induced in the skin of rats by the feeding for four months of a diet deficient in essential fatty acids. The concentration of neutral lipids increased in the experimental skin specimens with the exception of free cholesterol. Analysis of fatty acids in the skin lipids of these essential fatty acid deficient rats showed a marked increase in monoenoic and eicosatrienoic acids, with a concomitant decrease in linoleic and arachidonic acids. Incubation of skin specimens from the essential fatty acid deficient rats with [2-3H]glycerol and [1-14C]acetate showed a marked increase in the incorporation of both precursors into all lipid classes. Particularly, their incorporations into phosphatidylcholine were predominant compared to other lipid classes. With regard to the molecular species of phosphatidylcholine, saturated-monoenoic and monoenoic-monoenoic species were highly synthesized in the skin from essential fatty acid deficient animals, and the synthesis of saturated-dienoic and tetraenoic species was very low with either precursor. Significant decreases in these labelings were also noted in saturated-saturated species. Addition of prostaglandin E2 to the incubation medium did not significantly affect the metabolism of any of the lipid classes in the skin from the essential fatty acid deficient rats. The present results, therefore, suggest that phosphatidylcholine containing linoleic acid may be a key lipid in the epidermal barrier function.

Acetates↗
PubMed1996

Essential fatty acid deficiency and home total parenteral nutrition patients.

The requirements for essential fatty acids in patients on home parenteral nutrition are not well described. We therefore studied the needs of 12 patients receiving parenteral nutrition for at least 4 mo (range: 4 mo-17.3 yr; mean 7.0 +/- 5.2 yr). Prior to the study, each patient had been receiving intravenous lipids either weekly or biweekly and had a triene to tetraene ratio (TTR) on plasma phospholipids performed at least annually. A TTR > or = 0.2 was considered diagnostic for essential fatty acid deficiency (EFAD). The purpose of this study was to determine the required intravenous lipid supplementation in patients on home total parenteral nutrition (HTPN). Patients with an initial TTR of < 0.2 had their intravenous lipid stopped and changes in their serum phospholipid fatty acids were followed every 3-4 wk. Nine of 12 patients had TTRs > 0.2 at some point in the study. Phase I consisted of patients who at initiation of the study had normal TTRs and were taken off lipid supplementation until their TTR became abnormal. Phases II, III, IV, and V consisted of lipid delivered in total nutrient admixtures in biweekly doses of 0.6, 1.2, 1.8, and 2.4 g of fat/kg bodyweight, respectively. Eight patients normalized their TTRs on the biweekly lipid regimens; one patient expired before his ratio normalized; and three patients could not be made deficient in essential fatty acids after 26 or more wk of fat-free parenteral nutrition. Most patients required 1.2 to 2.4 g of lipid/kg bodyweight/biweekly to correct serologic EFAD. The clinical background, as well as the length of small bowel remaining, did not seem to identify those patients who required lipid supplementation nor the final dose of lipid needed to normalize their TTRs.

Adult↗
PubMed1986

Effects of essential fatty acid deficiency on mitochondria and peroxisomes in rat hepatocytes with special reference to a partially hydrogenated fish oil diet.

Feeding male rats a high cal% partially hydrogenated fish oil diet induced morphological and biochemical changes in hepatocytes at the mitochondrial and peroxisomal level. At the mitochondrial level, formation of megamitochondria was related to the development of an essential fatty acid deficiency, as measured by a high 20:3/20:4 fatty acid ratio. These mitochondrial changes were fully prevented by adding linoleic acid to the partially hydrogenated fish oil diet. The megamitochondria revealed a normal specific content of respiratory chain pigments, normal specific respiratory rates and a normal energy coupling. At the peroxisomal level, feeding of the partially hydrogenated fish oil diet caused a considerable proliferation, which was unrelated to essential fatty acid deficiency. The total number of peroxisomes increased 1.9-fold, and 2.6-fold in the presence of added linoleic acid. Essential fatty acid deficiency seemed to result in an inhibition of peroxisomal biogenesis. It was concluded that the induction of megamitochondria by partially hydrogenated fish oil was fully attributable to essential fatty acid deficiency, whereas peroxisomal proliferation must be attributed to other factors in the diet.

Animals↗
PubMed1985

Safflower oil emulsion administration during parenteral nutrition in the preterm infant. 1. Effect on essential fatty acid status.

To determine the effect of a safflower oil emulsion on the essential fatty acid (EFA) status of preterm infants during parenteral nutrition, subjects were randomized to receive Liposyn at 0.34 g (group 1), 0.68 g (less than 0.5% of lipid from linolenic acid, group 2), or Modified Liposyn at 0.68 g/kg/day (5.0% of lipid from linolenic acid, group 3). Doses of 0.34 and 0.68 g of Liposyn provided linoleic acid in amounts equivalent to 2 and 4% of the estimated caloric requirement (120 cal/kg/day) and 5 and 10% of the actual caloric intake. No significant differences were detected in plasma phospholipid triene/tetraene ratios and arachidonic acid levels between groups 1 and 2 or between groups 2 and 3, respectively. Plasma phospholipid triene/tetraene ratio and arachidonic acid did not change in the lipid-supplemented group throughout the study period, but the former remained significantly lower (p less than 0.001) and the latter significantly greater (p less than 0.001) than in a reference group of infants who received fat-free parenteral nutrition. We conclude that Liposyn administration providing linoleic acid at 2 or 4% of the estimated caloric requirement or 5 or 10% of the actual caloric intake prevented any significant changes in essential fatty acid status from occurring. Moreover, linolenic acid supplementation at 5% of the total lipid intake did not appear to affect arachidonic acid synthesis in the preterm infant.

Arachidonic Acid↗
PubMed1976

[Fetal and neo-natal development of brown adipose tissue in guinea pigs and rats. Feto-maternal or milk transfer of essential fatty acids : lipogenesis and morphology (author's transl)].

Brown adipose tissue (BAT) lipogenesis (fatty acid, glycerol and CO2 synthesis) and its morphology determined by optical microscopy, were studied in guinea pigs and rats during intra-uterine life and during the suckling period. Following the receptor induction and after the commencement of the hormone sensitive adenylate-cyclase/lipase system (i.e. on the 60th day in guinea pigs, on the 20th day in rats), the fetal BAT releases fatty acids (NEFA) and is capable of allowing the non-shivering thermogenesis. When the maternal diet and, consequently, the fetal or neonatal BAT are supplied with considerable linoleic acid, NEFA contain a large proportion of essential fatty acids. In vitro, the greater the linoleic acid concentration in these NEFA, the less inhibited is the lipogenesis from (2-14C) pyruvate. Thus, in periods just preceding or succeeding birth, fatty acid and glycerol synthesis are higher when the feto-maternal and/or the milk supply are enriched in linoleic acid than when they contain a large proportion of endogenous fatty acids. Morphological studies indicate that the adipose cell evolution could be nonidentical in BAT more or less enriched in essential fatty acids. Linoleic enriched BAT (of animals born to females kept on a sunflower oil diet) seemed to be in a healthy physiological state at birth, perhaps due to rapid lipid renewal and synthesis in their membranes. The control BAT (of animals born to females kept on a lard diet) appeared loaded with fats and in a worse conservation state at the same age.

Adipose Tissue, Brown↗
PubMed1983

Essential fatty acids in the serum and cerebrospinal fluid of multiple sclerosis patients.

Statistical evaluation of essential fatty acids (determined by gas chromatography) in the serum and cerebrospinal fluid of patients with definite MS and acute CCT showed marked differences as compared to healthy subjects. It was also evident that the decrease of essential fatty acids in MS patients differed from that of CCT patients. Whereas the fatty acid levels in the serum of MS patients revealed only minor differences as compared to the controls and CCT patients, MS patients did show a clear decrease, especially of linoleic and arachidonic acids, in the CSF. This difference was most pronounced in cholesterol esters in the CSF. One absorption study with safflower oil demonstrated normal enteral absorption of essential fatty acids and the ability to cross the blood-CSF barrier.

Acute Disease↗
PubMed1980

[Essential fatty acids in cardiovascular physiopathology].

Numerous studies have shown that a limitation of dietary saturated fatty acids and cholesterol associated with an increase in linoleic acid consumption lowers high blood cholesterol level (a risk factor in the development of atherosclerosis). Besides the importance of dietary fatty acid composition in determining blood lipoprotein concentrations, it has been shown that increased intake of dietary linoleic acid influences arterial thrombosis tendency in rats and improves blood platelet function in man. Linoleic acid rich diets also loffer arterial blood pressure in salt loaded rats and in hypertensive men. Moreover, these diets improve heart function in rats as measured by coronary perfusion rate and ventricular work. These favourable effects of linoleic acid on various risk factors of cardiovascular diseases are observed at dietary levels which largely exceed the minimum amount required to prevent or cure the essential fatty acid deficiency syndrome. It is evident that the study of the physiological effects of linoleic acid goes beyond the scope of this syndrome. Essential fatty acids have structural functions as integral part of membrane phospholipids and dynamic functions as precursors of prostaglandins. On account of their structural function, the essential fatty acids influence the fluidity of biomembranes and the activity of membrane-bound enzymes and receptor systems. Certain physiological effects of dietary linoleic acid would be explained via this mechanism. Moreover linoleic acid is known to regulate the endogenous prostaglandin biosynthesis. Though incomplete, the knowledge gained fully justifies the application of preventive measures proposed by numerous expert committees for groups of populations with a high rate of atherosclerosis.

Animals↗
PubMed1997

Essential fatty acids and their trans geometrical isomers in powdered and liquid infant formulas sold in Canada.

BACKGROUND: Animal and human studies have suggested that trans fatty acids might alter some physiological functions and adversely affect the growth and essential fatty acid balance of infants. In this context it is important to know the fatty acid composition, including the levels of trans isomers of oleic, linoleic and alpha-linolenic acids in infant formulas. METHODS: Ten liquid and fourteen powdered formulas for term infants were purchased from retail stores in Canada. The fatty acid composition of each formula was determined by capillary gas-liquid chromatography. RESULTS: All the formulas met the minimum content of 500 mg of linoleic acid/100 kcal formula (equivalent to 4.5% of energy) specified under current Canadian regulations. The formulas all met the minimum energy levels of 3% as linoleic acid and 0.7% as alpha-linolenic acid recommended recently by an ad hoc committee of Health Canada. However, in nine formulas, the proportion of linoleic acid was more than 20% of total fatty acids, and consequently, in five of them, the ratio of linoleic acid to alpha-linolenic acid exceeded the maximum ratio of 16:1 recommended by the ad hoc committee. Trans fatty acids were present in all the samples, and generally the liquid formulas displayed a higher total trans content (mean 1.9%, range 0.9-3.1%) than powdered formulas (mean 1.4%, range 0.6-2.5%). The amounts of trans isomers of linoleic and alpha-linolenic acids and the degree of isomerization of these fatty acids were also higher in liquid formulas than in powdered formulas. CONCLUSIONS: A few of the Canadian infant formulas would provide one-third of alpha-linolenic acid as trans geometric isomers.

Canada↗
PubMed1997

Fatty acid composition, eicosanoid production and permeability in skin tissues of rainbow trout (Oncorhynchus mykiss) fed a control or an essential fatty acid deficient diet.

Rainbow trout (Oncorhynchus mykiss) were fed either a control diet containing fish oil or an essential fatty acid (EFA) deficient diet containing only hydrogenated coconut oil and palmitic acid as lipid source (93.4% saturated fatty acids) for 14 weeks and the fatty acid compositions of individual phospholipid classes from skin and opercular membrane (OM) determined. The permeability of skin and OM to water and the production of eicosanoids in skin and gills challenged with the Ca2+ ionophore A23187 were also measured. Phospholipid (PL) fatty acid compositions were substantially modified in EFA-deficient fish, with increased saturated fatty acids and decreased polyunsaturated fatty acids (PUFA), especially arachidonic acid (AA) and eicosapentaenoic acid (EPA), while docosahexaenoic acid (DHA) was largely retained. The onset of EFA deficiency was shown by the appearance of n-9 PUFA, particularly 20:3n-9. The main effects of EFA deficiency on phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were to increase saturated fatty acids and monoenes, especially 16:1 and 18:1, and to decrease EPA and DHA. The content of DHA in phosphatidylserine (PS) was high in control animals (40% in skin and 35% in opercular membrane) and was mostly retained in EFA deficient animals. Arachidonic acid (AA) was the most abundant PUFA esterified to phosphatidylinositol (PI) and was significantly reduced in EFA deficient animals (from 31% to 13% in skin), where a large amount of 20:3n-9 (9% in skin) was also present. Influxes and effluxes of water through skin and opercular membrane were measured in vitro. No differences were detected between rainbow trout fed the control or the EFA deficient diet. 12-Hydroxyeicosatetraenoic acid (12-HETE), 12-hydroxyeicosapentaenoic acid (12-HEPE) and 14-hydroxydocosahexaenoic acid (14-HDHE) could not be detected in skin from control or EFA deficient fish. There was no difference between control and EFA deficient trout in the levels of leukotriene C4 (LTC4) and leukotriene C5 (LTC5) in skin cells challenged with the calcium ionophore A23187, and of prostaglandin F2alpha (PGF2alpha), 12-HETE and 12-HEPE in gill cells challenged similarly. Prostaglandin F3alpha (PGF3alpha) production by ionophore stimulated gill cells was significantly reduced in fish fed the EFA-deficient diet. 14-HDHE produced by gill cells was 3.3 fold higher in EFA deficient fish compared to controls.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1977

Metabolism of gamma-linolenic acid in essential fatty acid-deficient rats.

Female rats were weaned and fed a semipurified diet lacking in essential fatty acids. After 160 days, the deficient diet was supplemented with varying amounts of gamma-linolenic acid. Changes in body weight and feed efficiency were measured. Total liver phospholipid fatty acids were also analyzed. Supplementation with gamma-linolenic acid to the deficient diet for 7 days led to improvements in body weight and feed efficiency of the deficient rats. The liver phospholipid fatty acid composition returned to a normal pattern. There was a reduction of 5,8,11-eicosatrienoic acid and an increase in the arachidonic acid. Thus, there was a fall in the triene: tetraene ratio with increasing dietary supplementation of gamma-linolenic acid. The essential fatty acid potency, the minimum dietary requirement for this fatty acid, and the widely accepted levels of the minimum requirements of dietary essential fatty acids are discussed.

Animals↗